Drugs online research references
Pediatr Res. 1990 Apr;27(4 Pt 1):332-6.
Reduction of perinatal hypoxic-ischemic brain damage with allopurinol.
Palmer C, Vannucci RC, Towfighi J.
Department of Pediatrics, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
Cytotoxic free radicals are generated during cerebral hypoxia-ischemia and reperfusion. We studied the efficacy of allopurinol, a xanthine oxidase inhibitor and free radical scavenger, in reducing posthypoxic-ischemic damage in the developing brain of 7-d-old rat pups. Hypoxic-ischemic injury to the right cerebral hemisphere was produced by ligation of the right common carotid artery followed by 3 h of hypoxia with 8% oxygen. Thirty to 45 min before the hypoxia, the rats received either allopurinol (dose = 130-138 mg/kg) or an equal vol of saline (0.2 mL). Some pups were killed at 42 h of recovery for measurement of cerebral hemispheric water content, whereas others were killed at 30 or more d for neuropathologic examination. A total of 18 allopurinol treated rats had significantly less water content in the right hemisphere (89.07 +/- 0.32%) than 23 saline-treated animals (91.64 +/- 0.25%, mean +/- SEM, p less than 0.0001). Rank scoring of neuropathologic alterations revealed that the allopurinol treated rats were less damaged (p = 0.001). Only two of 13 brains from the allopurinol group suffered infarction compared to 10 of the 14 saline-treated animals. The results indicate that allopurinol reduces both cerebral edema and the extent of perinatal hypoxic-ischemic brain damage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2342827&dopt=Abstract
Liver. 1999 Feb;19(1):42-9.
Direct cytotoxicity of hypoxia-reoxygenation towards sinusoidal endothelial cells in the rat.
Blanc MC, Housset C, Lasnier E, Rey C, Capeau J, Giboudeau J, Poupon R, Vaubourdolle M.
Service de Biochimie A, INSERM U402 Hopital Saint-Antoine, Paris, France.
AIMS/BACKGROUND: Sinusoidal endothelial cells are the primary target of ischemia-reperfusion injury following liver preservation. The present study was undertaken to examine the susceptibility of sinusoidal endothelial cells to hypoxia-reoxygenation and the potential role of oxygen free radicals in the induction of cell injury. METHODS: Sinusoidal endothelial cells were isolated from rat liver. After 2 3 days of primary culture, the cells were exposed to hypoxia (N2/CO2 95/5) for 120 min and reoxygenation (O2/CO2 95/5) for 90 min. Control cells were exposed to hypoxia alone, to 95% O2 alone or were maintained under normoxic conditions. Human umbilical vein endothelial cells were used as a model of vascular endothelial cells and submitted to the same protocol. Cell viability and lipid peroxidation were assessed by LDH leakage and malondialdehyde production, respectively. In order to test the potential role of xanthine oxidase and mitochondrial dysfunction in cell injury, the cells were treated with allopurinol and potassium cyanide (KCN) respectively. RESULTS: The different gaseous treatments did not affect LDH leakage in human umbilical vein endothelial cells. In sinusoidal endothelial cells, the sequential hypoxia-reoxygenation caused a significant increase in LDH release, malondialdehyde production and xanthine oxidase activity while hypoxia alone had no effect except on xanthine oxidase activity. Allopurinol inhibited xanthine oxidase without preventing cell injury or lipid peroxidation in this latter cell type. CONCLUSIONS: The results suggest that sinusoidal endothelial cells, as opposed to vascular endothelial cells, are susceptible to a direct cytotoxic effect of hypoxia-reoxygenation. This effect occurs in combination with an increase in xanthine oxidase activity and lipid peroxidation, although cell injury is mediated at least in part by mechanisms independent of xanthine oxidase such as mitochondrial dysfunction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9928765&dopt=Abstract
Tropenmed Parasitol. 1975 Jun;26(2):232-8.
Comparison of tritiated hypoxanthine, adenine and adenosine for purine-salvage incorporation into nucleic acids of the malarial parasite, Plasmodium berghei.
Van Dyke K.
This study was accomplished to examine the relative importance of different metabolic precursors of nucleic acid synthesis in the malarial parasite, P. berghei. Three possible pathways for incorporation of Adenine (type) compounds exist: 1) incorporation via hypoxanthine, 2) via adenine, or 3) via adenosine. The parasitized cell and erythrocyte-free malarial parasite were both examined because of possible metabolic differences that could be encountered. Hypoxanthine was clearly the best precursor at both levels with extra-incorporation in the presence of allopurinol (10(-4)M), which protects oxidative metabolism of hypoxanthine. Adenosine was less efficient in its incorporation into nucleic acids at both levels. Adenine was clearly the poorest precursor being extremely less efficient compared to hypoxanthine 1/50 at parasitized cell level and 1/100 at the free parasite level. At both levels adenine seemed to be slightly more efficient in the presence of allopurinol and this appeared to be a similar to the incorporation via adenosine with allopurinol. In both cases, part of the incorporation could be coming via conversion to hypoxanthine because allopurinol protects oxidation of hypoxanthine via inhibition of xanthine oxidase. With the prior observation of Manandhar and Van Dyke that adenosine is converted to hypoxanthine outside or on the surface of the malarial parasite one is lead to conclude that of the three pathways the hypoxanthine pathway is probably the major and possibly the almost totally important pathway making hypoxanthine's uptake and/or conversion to inosine monophosphate a key event of metabolic and chemotherapeutic importance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1099747&dopt=Abstract
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